A group of researchers led by the Complutense University of Madrid (UCM), together with the Jiménez Díaz Foundation, has obtained encouraging results by testing in mice with diabetic retinopathy an experimental treatment based on the molecule MiS1, associated with type 2 diabetes.
The authors point out that diabetic retinopathy is one of the complications of diabetes that can ultimately seriously damage the retina. Normally emphasis is placed on deterioration of blood vessels, but the disease also affects the nerve cells of the retina and modifies their inflammatory response.
"These changes may appear before there are obvious vascular lesions. Our study focuses on that phase of the disease, which could offer new opportunities to protect the retina," highlighted Elena Salobrar-García, a researcher in the Department of Immunology, Ophthalmology and ORL and in the Ramón Castroviejo Institute of Ophthalmological Research.
The work, published in the journal "Investigative Ophthalmology & Visual Science", analyzes the therapeutic potential of MiS1 as the basis for a future drug. It is a peptide, that is, a small chain of amino acids, designed to reproduce part of the function of SOCS1, a protein involved in regulating inflammatory signaling.
Over a period of seven weeks, the team administered MiS1 to mice with type 2 diabetes and examined in detail the changes produced in their retinas. In diabetic animals that received no intervention, a clear neurodegenerative process was detected: the retina appeared thinner, a reduction in ganglion neurons was recorded, and alterations in microglia were observed, the cells of the nervous system responsible for reacting to tissue damage.
"In contrast, the mice treated with MiS1 showed less thinning of the retina and changes in the shape of microglial cells," says the UCM researcher.
The trial also included another group of mice that received baricitinib, a drug that interferes with certain signaling pathways related to inflammation, where protective effects on nervous tissue were likewise detected. In both treated groups, a greater number of ganglion neurons was counted than in untreated diabetic mice, although this difference reached statistical significance only in the group that received baricitinib.
"The interest for patients lies in the possibility of acting on disease processes that current treatments do not directly address. Today, many treatments are aimed at vascular complications, such as abnormal growth of blood vessels or the accumulation of fluid in the retina," Lucas Opazo, researcher at the Instituto de Investigación Sanitaria Fundación Jiménez Díaz, has explained.
New studies are required before applying it in humans
The people responsible for the work emphasize that, if subsequent research confirms that modulating inflammation contributes to preserving retinal neurons and visual function, strategies could be considered to intervene in earlier stages or to complement the therapies that are already used in clinical practice.
"There is still an important path to go. These results have been obtained in mice and we have not checked whether any of the treatments improves vision. We also do not know if it will be effective and safe in people. The next step is to study in greater detail how it acts and whether the protection we have observed in the structure of the retina translates into protection of its function," concludes Salobrar-García.